Common esophageal diseases that are commonly missed (Proceedings)


Regurgitation occurs when there is either an anatomic obstruction or a physiologic weakness in the esophagus. In either case, food is retained in the esophagus and, if it passively migrates back into the oropharynx, can be regurgitated. The problem should be diagnosed quickly in an attempt to solve it before the esophagus becomes irreversibly-dilated or the patient experiences an aspiration pneumonia.

Regurgitation occurs when there is either an anatomic obstruction or a physiologic weakness in the esophagus. In either case, food is retained in the esophagus and, if it passively migrates back into the oropharynx, can be regurgitated. The problem should be diagnosed quickly in an attempt to solve it before the esophagus becomes irreversibly-dilated or the patient experiences an aspiration pneumonia.

First, be sure to try to distinguish vomiting from regurgitation. We usually start doing this by considering the history and physical examination. This can be hard to do, and the following are guidelines only — some animals that clearly appear to be vomiting are in fact regurgitating and vice-verse. In particular, it is very easy for a vomiting dog to appear to be regurgitating. However, these guidelines are still useful and usually point us in the correct direction.

  • Prodromal nausea is commonly found with vomiting. Since vomiting is a centrally-mediated response, other signs such as salivating, discomfort and "gurgling" stomach are often seen beforehand. Many animals that are about to vomit will pace, whine or show some sort of anxiety or discomfort. With regurgitation the animal may be sitting and suddenly "gag" up some material. In general, animals know that they are going to vomit, but they are often unaware that they are going to regurgitate until they actually start doing it. Sometimes the regurgitation is as much a surprise to them as it is to the client. These are not absolutes - animals don't always read the book.

  • Retching typically follows prodromal nausea and is characterized by forceful, abdominal contractions in animals that are vomiting. (You will see some abdominal contractions with regurgitation but they are not severe or forceful and they do not tend to be repetitive.) If you're not sure what retching is like, just think back to the last time you had to vomit. Don't just ask owners "Did the animal retch?" because they may consider any contractions of the abdomen to be retching. Clearly describe precisely what you mean so that they can give you an accurate answer.

  • The material the animal expels sometimes help us distinguish what is going on. If possible, let the client describe the material first so they're not just agreeing with you to make you happy. So-called "undigested" material can be either vomited or regurgitated. If it is digested, then this would indicate that the material came from either the stomach or intestines; however, it can be very difficult or impossible to visibly differentiate undigested material that was chewed up, mixed with mucus and saliva and has been sitting in the esophagus for a long time from digested material.

     Mucus can come from either the salivary glands (i.e., the regurgitating animal) or the stomach (i.e., the vomiting animal).

  • Red blood can be seen with either vomiting or regurgitation, but semi-digested blood that looks like coffee grounds is only seen with vomiting. However, finding digested blood does not ensure that the bleeding originated in the stomach.

     Bile indicates that the material is from the stomach or intestines. Bile is a green, yellow or dark brown color. Don't just ask if the animal is vomiting bile; many clients assume that vomitus contains bile (i.e., my animal "vomited", therefore it must have vomited bile). Clearly describe what you mean by "bile".

  • The amount of material ejected from the mouth varies from large to small with both vomiting and regurgitation. Likewise, the timing of the episode relative to eating can vary from immediately after eating to 1 ½ days after the last meal, regardless of whether the animal is vomiting or regurgitating. Don't forget that you can regurgitate mucus even though you have not eaten for days.

If you are still confused as to whether the patient if vomiting or regurgitating, the most definite method of distinguishing vomiting from regurgitation usually consists of performing plain thoracic radiographs, possibly followed by a barium contrast esophagram. There are some causes of regurgitation that will be missed by such studies, but they are far and few between.

Physical examination may also help distinguish vomiting from regurgitation. Occasionally the esophagus is so dilated and flaccid that it can be seen expanding and collapsing near the thoracic inlet as the animal breathes (much like a bellows). A particularly nice trick is to test the expelled material with a urine dipstick. If the pH of the material that the animal spit out is < 5 or if bile is present, then the material has been vomited. Otherwise, it has probably been regurgitated. Do not trust the reaction for blood. It is invariable positive and does not help distinguish vomiting from regurgitation.

Initial diagnosis:

The first consideration in the animal that is regurgitating is to clarify whether the regurgitation is due to anatomic obstruction of the esophagus or due to esophageal weakness. A barium-contrast esophagram is the best way to determine which is occurring, and is often indicated in patients with suspected esophageal disease. Plain thoracic films should be done first because they will often reveal esophageal foreign objects, pneumothorax, and/or pleural effusion; signals that a contrast procedure is not needed and in fact is contraindicated. However, a contrast procedure is otherwise useful, even if plain films strongly suggest megaesophagus (i.e., an obvious air-filled, dilated esophagus). Some animals with aerophagia have plain radiographic findings suggesting esophageal weakness, but the contrast procedure will demonstrate normal esophageal function. I absolutely avoid using barium paste because it can seemingly cause worse problems than liquid barium if it is aspirated.

Esophageal foreign objects usually consist of bones but may be rawhide treats, toys, balls, rocks, wood, etc. They usually lodge at the thoracic inlet, base of the heart, or lower esophageal sphincter. A history of a patient that begins to regurgitate (as opposed to vomit) acutely is very suggestive of acquired esophageal obstruction due to a foreign object. These patients may continue to drink water, but they typically refuse solid food because the food bolus cannot pass by a partial esophageal obstruction and causes pain whenever it tries to. A casual, careless history that fails to raise the suspicion of regurgitation will typically lead the clinician to suspect an acute gastritis. However, the realization that the patient is regurgitating (as opposed to vomiting) should be a "red flag". Too often, a pet which has ingested a foreign object is treated conservatively while we wait and see if the supposed gastritis spontaneously resolves. If an animal starts to vomit acutely, it could have any number of diseases. But, if an animal starts to regurgitate acutely, then esophageal foreign object is your primary rule out.

Plain radiographs should be performed first. Bones are a common cause of obstruction, and plain films that are made with proper technique and then carefully evaluated are diagnostic in most cases. (Remember that we are often looking for poultry bones which are not as radiodense as the patient's bones – this means that excellent radiographic technique is required to see them radiographically.) If plain films are not diagnostic, then contrast films are needed. However, an ill-defined fluid density in the region of the esophagus, pleural effusion, or pneumothorax may be very suggestive of esophageal perforation and mediastinitis. If none of these findings are present, barium is the preferred contrast agent. Esophageal perforation may occur at variable times after ingestion of a foreign object. Even a blunt object, if tightly lodged in the esophagus, can cause ischemia and perforation in 2-3 days. The prognosis for animals with esophageal perforation and severe mediastinitis is guarded to poor, depending upon their condition at the time of diagnosis. Major points to remember: Good quality plain radiographs are usually diagnostic and endoscopy is almost always the preferred method of therapy.

Foreign objects, even fish hooks, can often be successfully removed endoscopically. It is preferable to use a rigid alligator forceps to pull the object into a rigid endoscope and then withdraw it and the scope as a unit. If a large object or a bone cannot be easily dislodged, do not force it lest you perforate a previously intact esophagus. Fish hooks have usually penetrated the mucosa (and sometimes the muscular tunics); you will often have to use rigid equipment to carefully force the tip of the hook back out of the mucosa. A small hole is left, but there are very seldom any complications. Do not push large objects or bones into the stomach unless you are sure that it is smooth on the aborad side and will not further damage the mucosa. Finally, be careful if you insufflate the esophagus lest you rupture a weakened area in the mucosa and/or cause a fatal tension pneumothorax. After removing the foreign object, retake plain chest radiographs to be sure that a pneumothorax (which would indicate a perforation) is not present. Antibiotics are indicated if there is substantial esophageal mucosal ulceration (and especially if you remove a fish hook which had been used with various baits that can harbor anaerobic bacteria). Depending upon the amount of damage, corticosteroids may be used to try to prevent cicatrix formation; however, it is not clear that they are effective. The vast majority of esophageal foreign objects can safely be removed endoscopically, especially with a rigid endoscope.

Cicatrix (i.e., scarring) may occur after an episode of severe esophagitis from any cause (including foreign objects). It is particularly easy to miss this problem on a barium swallow if only liquid barium is used. If radiographs using liquid barium are nonrevealing, repeat the study using barium mixed with food, which is more likely to stop at a partial obstruction. Endoscopy is very good at finding these lesions; however, you must keep in mind the size of the patient as you evaluate the esophageal lumen. A partial stricture will be very obvious in a 10 lb dog or cat but may not be apparent in an 85 lb animal. Balloon-dilatation or bouginage is usually effective; it is also more likely to be successful than surgery and resection of the affected area. In general, surgical resection should be a last ditch resort and only used if esophageal ballooning or bouginage has failed despite repeated dilatations. However, you must use proper esophageal balloons because Foley catheters and endotracheal tubes with inflatable cuffs will often not allow you to dilate a dense or mature stricture. More difficult cases (i.e., those with extensive strictures or with concurrent severe esophagitis) may benefit from a couple of techniques. Endoscopic administration of intralesional steroids may help minimize reformation of the stricture. Typically we put 1-2 ml of Vetalog at the site of the stricture either before or after ballooning. Another technique is to make 3-4 equidistant cuts into the stricture using an electrocautery device (i.e., either a snare or a knife) prior to ballooning. This helps the stricture to "break" open at multiple spots with the idea that there will be 3 or 4 smaller, less deep lacerations at the stricture site instead of one major, deep laceration which is more likely to restricture. However, you should not attempt to use cautery through an endoscope unless you have some training less you cause too much trauma to the tissues or destroy your endoscopic equipment.

Another technique is to "paint" the site where the stricture was broken down with Mitomycin C (NOT mithromycin C, there is a difference). A 5 mg bottle is reconstituted and soaked up into a gauze sponge. Then this sponge is endoscopically placed on the site where the stricture was broken up for 5 min. Then it is flushed off with 60 ml of water.

Finally, for particularly difficult cases, stents may be placed in the esophagus. These must be sutured in place. If an animal starts to have problems days to weeks after anesthesia, consider strongly the possibility that an esophageal stricture has developed secondary to esophagitis. If you are treating an esophageal stricture, remember that you may need to do 1-15 dilatations. If esophagitis is diagnosed, you need to treat it aggressively in order to help prevent the stricture from recurring quickly.

Esophagitis causes muscular weakness by interrupting the reflex arcs within the esophagus and/or between the esophagus and the brain. Severe esophagitis may be caused by anesthetic procedures in which animals are placed in dorsal recumbency and then have gastric acid pool in their esophagus for relatively long periods of time. However, gastroesophageal reflux from any cause can be responsible. Hiatal hernias occasionally are responsible for such reflux. Rare animals ingest caustic substances (e.g., lye), and some cats will like caustic disinfectants off their fur. However, a surprisingly large number of animals are administered caustic substances by veterinarians — specifically tetracyclines, NSAIDs, ciprofloxacin, and clindamycine. Pills and capsules are notorious for lodging in the esophagus of cats, and it is therefore not surprising that doxycycline is a recognized cause of esophageal stricture in cats. Esophagitis may also be secondary to any cause of protracted vomiting. In particular, parvovirus enteritis may cause such intense vomiting that esophagitis results. If a vomiting animal has the character of its vomitus change, which seems to suggest regurgitation, consider the possibility that esophagitis has occurred secondary to the persistent vomiting. Gastrinoma (a tumor which secretes gastrin and results in massive gastric acid secretion) also causes esophagitis because of the vast and unending amounts of acid the esophagus is exposed to as the dog continually vomits. Gastroesophageal reflux may be potentiated by or even caused by esophagitis (which may be caused by reflux in the first place). Thus, there may be a positive feedback loop which can be hard to break (i.e., esophagitis causes more reflux which causes more esophagitis which causes more reflux which causes ...). Barium esophagrams do not always reflect the severity of the esophagitis while esophagoscopy typically shows an edematous, reddened, bleeding esophageal mucosa, + structure formation. Esophagoscopy is the diagnostic method of choice to find esophagitis.

You should seek to prevent further gastroesophageal reflux by keeping the stomach as empty as possible by using prokinetics such as metoclopramide or, preferably, cisapride. Studies in people show that cisapride is clearly more effective than metoclopramide. The only real advantage of metoclopramide is that it can be given by injection; a useful fact in animals that are regurgitating profusely. In addition, gastric acid secretion should be minimized and preferably abolished. H-2 receptor antagonists (e.g., cimetidine, ranitidine, famotidine) suppress gastric acid secretion, but they do not eliminate it. This is because they are competitive inhibitors. That means that there is constantly some degree of competition between the H-2 receptor antagonists and the stimuli for acid secretion. Omeprazole, lanosprazole and pantoprazole are non-competitive inhibitors of gastric acid secretion. Therefore, these drugs can be noticeably more effective and can cause near gastric anacidity. You can try to achieve greater efficacy with the H-2 receptor antagonists by doubling or tripling their dose. Major points to remember: the more expensive therapy can be cheaper in the long run for patients with severe disease. Severe esophagitis needs to be treated aggressively.

A combination of omeprazole and cisapride seems to be the most effective medical treatment regime. Antibiotics are used to treat secondary infections, but nobody really knows if they do anything in this regard. Glucocorticoids have been thought to help retard fibrous connective tissue proliferation and cicatrix, but their effectiveness is uncertain (and they might predispose to infection). Placing a PEG tube seems to have some real advantages in patients with very severe disease. First, we will then know that the cisapride and omeprazole tablets will reach the stomach. Second, we will also know that the animal will receive its caloric and protein needs, and hopefully with less irritation to the esophagus than would have occurred otherwise.

If there is severe esophagitis, cicatrix may form and obstruction develop subsequently. Diagnosis of stricture is best accomplished by esophagoscopy IF the operator is familiar with such obstructions. It is surprisingly easy to pass a slender endoscope through a stricture and never recognize the stricture. It is also surprisingly easy to miss a partial obstruction due to a stricture with a barium esophagram. If you suspect a stricture and must use a barium esophagram to make the diagnosis, use barium mixed with solid food. Balloon-dilatation or bouginage is recommended if a stricture has occurred. Many animals need to have 2-6 dilatation procedures (all the while being treated for esophagitis), although some only need one procedure and some need more than 15. Do not try to resect the stricture unless you have had prior dilatation procedures fail.

Hiatal hernias may be more common than suspected. They can be difficult to diagnose, and one may need to put pressure on the abdomen during film exposure to try to push the stomach through the hernia and into the chest so that it can be diagnosed radiographically. Shar Pei's seem to have a relatively high incidence of hiatal hernias.

Acquired esophageal weakness is usually (but not always) easy to distinguish from obstruction radiographically, especially when a barium contrast radiograph is performed. However, the severity of the radiographic lesion (i.e., the degree of dilatation) does not always correlate well with the clinical severity. Acquired esophageal weakness is typically difficult to resolve because it is hard to find the underlying cause. Myopathy, neuropathy, myasthenia gravis, dermatomyositis, dysautonomia, esophagitis, Addison's disease, Spirocerca lupi, tick paralysis, central nervous system disease, or infiltrative non-obstructive esophageal tumors are possible causes. Generalized myopathies and neuropathies often affect the esophagus because it is composed of striated muscle in the dog. Signs of lower motor neuron disease in these patients are sometimes seen and can include loss of muscle mass, weakness, an inability to bark, or a change in the quality of the bark. Some clients report that their animal has laryngitis, which may seem likely because these pets typically have repeated respiratory infections due to aspiration pneumonia. Treatment of the myopathy or neuropathy should resolve the problem, but symptomatic therapy for the esophageal dilatation is indicated.

Generalized myasthenia gravis usually presents as weakness during exertion which resolves after resting; however, generalized myasthenia can present in a variety of ways, including apparent lameness or permanent weakness. Electromyography and assay for circulating antibodies to acetylcholine receptors are the most definitive tests. Localized myasthenia in the dog is a syndrome in which the esophagus is the only muscle which is obviously weak. Up to 25-30% of dogs with acquired esophageal weakness have this syndrome. Third degree heart block may also be seen in some patients with megaesophagus due to myasthenia. This is diagnosed in dogs with esophageal weakness by detecting serum antibodies to acetylcholine receptors. The antibodies are relatively stable and require little special handling other than refrigeration. If myasthenia is strongly suspected but the titer is negative, it can be valuable to repeat the titer as they sometimes seroconvert later. You cannot perform an edrophonium response test to diagnose localized myasthenia. Myasthenia gravis will sometimes spontaneously resolve. Treatment for myasthenia gravis that does not spontaneously resolve may include anti-acetylcholinesterase drugs, corticosteroids and/or cytotoxic agents. Azathioprine and mycophenolate seem to be effective drugs for this purpose. In general, we try to avoid steroids as they seem to be associated with more problems. In really severe cases, we can place a percutaneous gastrostomy tube to support the patient and lessen aspiration whle waiting for the drugs to have an effect. However, a gastrostomy tube will not prevent all aspiration as the dog is still swallowing saliva which can be regurgitated and aspirated.

Hypoadrenocorticism may be responsible for causing esophageal weakness, even when the serum electrolytes are normal. This is especially true in standard sized, black poodles, but it can occur in any breed. Treatment for hypoadrenocorticism is steroids, which can make the esophagus start functioning again. However, if your diagnosis is wrong and you give steroids because you suspect the dog may have hypoadrenocorticism, all you are doing is making aspiration pneumonia and subsequent death that much more likely.

Idiopathic megaesophagus (i.e., either congenital megaesophagus or acquired megaesophagus for which a cause cannot be found) can only be treated with symptomatic therapy, which usually consists of feeding the animal 3-4 meals of gruel from an elevated platform and making the pet remain in the near vertical position from 5-10 minutes after eating. Near-vertical means just that. It is useless for the dog to just lift its head up while eating; it should be standing on its back legs. If necessary, use a portable ladder or put the dog in a large trash can to help it remain vertical during this time. This approach is a time-honored treatment, but it does not always work. Some animals with idiopathich esophageal weakness are controlled as well (or better) if they are fed free-choice dry food from an elevated platform. Some can even be fed from the floor. Free-choice feeding encourages the pet to eat small amounts of food throughout the day, thus avoiding intermittent large meals which are more likely to be retained and further dilate the esophagus. If there is any esophageal motility remaining, the dry food may be easier for the esophagus to propel then gruel. It is difficult to predict which feeding regime will work best for a particular patient, and both of these feeding regimes may need to be tried. While most dogs with idiopathic megaesophagus die from aspiration, there are enough of them that respond well that it is very much worth trying. A reasonable percentage of dogs with idiopathic, congenital megaesophagus will spontaneously improve and have normal or near normal function. You cannot predict response to therapy or spontaneous remission; all you can do is support the patient and see what happens.

Some individuals have tried using cisapride in selected patients with idiopathic esophageal weakness that do not respond well to nutritional modification. Theoretically, cisapride would not be expected to work in these animals because cisapride primarily works on smooth muscle and canine esophagus is striated muscle. Furthermore, cisapride is expected to tighten up the lower esophageal sphincter, thus making it harder for food to pass out of the esophagus and into the stomach. Perhaps cisapride helps patients when gastroesophageal reflux is part of the problem.

Some owners elect to have a permanent gastrostomy tube placed in the patient. This will not eliminate all regurgitation or aspiration, because the patient is still swallowing saliva which will remain in the esophagus until it is regurgitated. However, gastrostomy tubes will help eliminate most of the regurgitation and can markedly prolong such a patient's quality, comfortable life.

Aspiration pneumonia is a major problem and cause of death in dogs and cats with esophageal weakness causing regurgitation. If the respiratory disease cannot be stopped by alleviating the regurgitation by dietary therapy, then it must be controlled by antibiotics. A transtracheal wash with cytology and culture will help identify optimal antibiotics. Until culture results are known, use of broad-spectrum, bactericidal drugs (i.e., amikacin plus either cephalothin or amoxicillin; enrofloxacin plus amoxicillin or clindamycin) are used. In severe cases of aspiration pneumonia, one may have to bypass the esophagus with a gastrostomy tube to prevent further aspiration. These tubes can be place with the aid of a flexible endoscope and be used for days to months.

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